Obesity has reached global epidemic proportions and there is therefore much need to understand mechanisms underlying excessive and uncontrolled food intake. Ghrelin, the only known circulating orexigenic hormone, stimulates feeding behavior via its CNS actions. In addition to its role in “metabolic hunger”, ghrelin potently increases food reward behavior (1,2). The neurochemical circuitry that links ghrelin to the mesolimbic reward system and to the increased food reward behavior remains unclear (3). Ghrelin receptors can be found on the ventral tegmental area (VTA) dopamine neurons (4) and ghrelin injection to the VTA is sufficient to drive food motivated behavior (5). It is, however, unknown which dopaminergic projections are relevant for ghrelin’s effects on reward, since VTA dopamine neurons send projections to several brain areas relevant for reward behavior including the nucleus accumbens (NAc), amygdala and prefrontal cortex. Here we examine whether VTA-NAc dopaminergic signalling is required for the effects of ghrelin on food reward and intake. To measure food motivation/reward behavior, rats were trained in a progressive ratio sugar-induced operant behavior schedule. Chow intake was measured subsequent to the operant behavior test. A D1-like or a D2 receptor antagonist was injected into the NAc in combination with ghrelin microinjection into the VTA to investigate whether this blockade attenuates ghrelin-induced food reward behavior. VTA injection of ghrelin significantly increased food reward behavior and chow intake. Pretreatment with either a D1-like or D2 receptor antagonist into the NAc, completely blocked the reward effect of ghrelin, leaving chow intake intact. We also found that this circuit is potentially relevant for the effects of endogenously released ghrelin as both antagonists reduced fasting (a state of high circulating levels of ghrelin) elevated sucrose-motivated behavior but not chow hyperphagia. Taken together our data identify the VTA to NAc dopaminergic projections, along with D1-like and D2 receptors in the NAc, as essential elements of the ghrelin-responsive circuits controlling food reward behavior. Interestingly the results also suggest that food reward behavior and the intake of chow are controlled by divergent circuitry, where NAc dopamine plays an important role in food reward but not in food intake. The idea that ghrelin’s effects on food intake and food reward behavior engage different reward circuitry is also supported by previous studies in which we were able to parse ghrelin’s effects these behaviors pharmacologically using mu-preferring opioid receptor antagonist or an NPY Y1 receptor antagonist (6).